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Protection against or triggering of Type 1 diabetes? Different roles for viral infections.

机译:预防或引发1型糖尿病?病毒感染的作用不同。

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摘要

The emergence of autoreactivity that ultimately destroys insulin-producing beta-cells and causes Type 1 diabetes (T1D) is a result of genetic susceptibility and environmental factors, such as viral infections. The ability to induce strong cellular immune responses and to cause inflammation in the target organ makes viral infections prime candidates for the initiation of islet autoreactivity. Indeed, certain viruses have been linked to the occurrence of T1D based on epidemiological, serological and histological findings; and several rodent studies clearly demonstrate that viral infections can trigger autoimmunity. However, viruses have also been shown to efficiently prevent autoimmunity, which underlines the beneficial aspects of exposure to microbial agents as suggested by the hygiene hypothesis. Here, we will try to untangle some aspects of the complex interplay between viruses and the immune system and we will recapitulate by what rationale certain viruses have been associated with T1D.
机译:自身反应性的出现最终破坏了产生胰岛素的β细胞并导致1型糖尿病(T1D),是遗传易感性和环境因素(例如病毒感染)的结果。诱导强烈的细胞免疫反应并在靶器官中引起炎症的能力使病毒感染成为引发胰岛自身反应性的主要候选药物。实际上,根据流行病学,血清学和组织学发现,某些病毒与T1D的发生有关。几项啮齿动物研究清楚地表明,病毒感染可以触发自身免疫。但是,还显示出病毒可有效预防自身免疫,这突出了卫生假设所建议的暴露于微生物制剂的有益方面。在这里,我们将尝试弄清病毒与免疫系统之间复杂相互作用的某些方面,并根据某些病毒与T1D相关的原理进行概括。

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